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  • 1
    Online Resource
    Online Resource
    Fasting confers stress resistance to skeletal muscle stem cells through non-metabolic actions of β- hydroxybutyrate: implications in cardioprotection and aging
    OAE Publishing Inc. ; 2022
    In:  The Journal of Cardiovascular Aging Vol. 2, No. 3 ( 2022), p. 34-
    Details
    In: The Journal of Cardiovascular Aging, OAE Publishing Inc., Vol. 2, No. 3 ( 2022), p. 34-
    Type of Medium: Online Resource
    ISSN: 2768-5993
    URL: Journal
    URL: Article
    DOI: 10.20517/jca
    DOI: 10.20517/jca.2022.24
    Language: Unknown
    Publisher: OAE Publishing Inc.
    Publication Date: 2022
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  • 2
    Online Resource
    Online Resource
    Nifedipine Attenuates Cardiac Hypertrophy by Inhibiting Nox4-induced Oxidation of HDAC4
    Elsevier BV ; 2014
    In:  Journal of Cardiac Failure Vol. 20, No. 10 ( 2014-10), p. S199-
    Details
    In: Journal of Cardiac Failure, Elsevier BV, Vol. 20, No. 10 ( 2014-10), p. S199-
    Type of Medium: Online Resource
    ISSN: 1071-9164
    URL: Article
    DOI: 10.1016/j.cardfail.2014.07.369
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2014
    detail.hit.zdb_id: 2048826-9
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  • 3
    Online Resource
    Online Resource
    Nifedipine Negatively Regulates Nox4 and Inhibits HDAC4 Oxidation in Phenylephrine-Induced Cardiac Hypertrophy
    Elsevier BV ; 2016
    In:  Journal of Cardiac Failure Vol. 22, No. 9 ( 2016-09), p. S207-
    Details
    In: Journal of Cardiac Failure, Elsevier BV, Vol. 22, No. 9 ( 2016-09), p. S207-
    Type of Medium: Online Resource
    ISSN: 1071-9164
    URL: Article
    DOI: 10.1016/j.cardfail.2016.07.290
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2016
    detail.hit.zdb_id: 2048826-9
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  • 4
    Online Resource
    Online Resource
    THE CELLULAR AND MOLECULAR RESPONSE OF CARDIAC MYOCYTES TO MECHANICAL STRESS
    Annual Reviews ; 1997
    In:  Annual Review of Physiology Vol. 59, No. 1 ( 1997-10), p. 551-571
    Details
    In: Annual Review of Physiology, Annual Reviews, Vol. 59, No. 1 ( 1997-10), p. 551-571
    Abstract: ▪ Abstract  External load plays a critical role in determining muscle mass and its phenotype in cardiac myocytes. Cardiac myocytes have the ability to sense mechanical stretch and convert it into intracellular growth signals, which lead to hypertrophy. Mechanical stretch of cardiac myocytes in vitro causes activation of multiple second messenger systems that are very similar to growth factor-induced cell signaling systems. Stretch of neonatal rat cardiac myocytes stimulates a rapid secretion of angiotensin II which, together with other growth factors, mediates stretch-induced hypertrophic responses in vitro. In this review, various cell signaling mechanisms initiated by mechanical stress on cardiac myocytes are summarized with emphasis on potential mechanosensing mechanisms and the relationship between mechanical loading and the cardiac renin-angiotensin system.
    Type of Medium: Online Resource
    ISSN: 0066-4278 , 1545-1585
    URL: Issue
    URL: Article
    DOI: 10.1146/physiol.1997.59.issue-1
    DOI: 10.1146/annurev.physiol.59.1.551
    RVK:
    WA 15000
    Language: English
    Publisher: Annual Reviews
    Publication Date: 1997
    detail.hit.zdb_id: 1474465-X
    SSG: 12
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  • 5
    Online Resource
    Online Resource
    Abstract 15378: Mitochondrial Fission Plays a Crucial Role in Cardiomyocyte Adaptation to Energy Stress via Mitophagy
    Ovid Technologies (Wolters Kluwer Health) ; 2014
    In:  Circulation Vol. 130, No. suppl_2 ( 2014-11-25)
    Details
    In: Circulation, Ovid Technologies (Wolters Kluwer Health), Vol. 130, No. suppl_2 ( 2014-11-25)
    Abstract: Mitochondria are dynamic organelles that undergo fusion and fission. This study aims to clarify the role of mitochondrial dynamics on energetic stress resistance in cardiomyocytes (CMs). Dynamin-related protein 1 (Drp-1) which mediates mitochondrial fission was localized primarily in the cytosol in CMs. Glucose deprivation (GD) induced modest mitochondrial accumulation of Drp1 in CMs within 4 hours. Four-hour GD increased the proportion of CMs with fused mitochondria (23.5±6.9 to 35.0±10.8%, p 〈 0.05), but also increased that of CMs with fission (2.1±0.3 to 15.5±4.8%, p 〈 0.05) in Ad-shScr-transduced CMs, whereas mitochondria with fission did not increase after GD in Ad-shDrp1-transduced CMs (0.3±0.6 to 0.8±0.5%). These results suggest that GD induces both mitochondrial fusion and fission, and Drp1 plays an essential role in mitochondrial fission in response to GD. Transduction with Ad-shDrp1 significantly increased TUNEL-positive CMs and reduced cell viability after 4 hours of GD compared to transduction with Ad-shScr, suggesting that endogenous Drp1 protects CMs against cell death during GD. We evaluated the role of Drp1 in mediating mitophagy using mitochondria-targeted Keima fluorescence. Keima has a bimodal excitation spectrum peaking at 440 and 560 nm, corresponding to the neutral and acidic pH states, respectively. Puncta with high 560/440, indicating the presence of mitochondria in lysosomes, were significantly increased after 4 hours of GD in CMs transduced with Ad-shScr, but not in CMs transduced with Ad-shDrp, suggesting that Drp1 is necessary for stimulating autophagic mitochondrial degradation. Next, we examined the role of fission on energy stress in vivo using cardiac specific Drp1 hetero knockout (Drp1-hetCKO) mouse. Translocation of Drp1 from cytosol to mitochondria significantly increased in response to 48-hour fasting in control mice but not in Drp1-hetCKO mice. Left ventricular ejection fraction did not change after fasting in control mice (79.8±6.4 to 78.6±8.3%). However that in Drp1-hetCKO mice decreased after GD (79.4±9.7 to 48.3±11.6%, p 〈 0.05), suggesting that Drp1 acts to preserve cardiac function during fasting. In conclusion, mitochondrial fission is crucial to adapt CMs to energy stress through mitophagy.
    Type of Medium: Online Resource
    ISSN: 0009-7322 , 1524-4539
    URL: Article
    DOI: 10.1161/circ.130.suppl_2.15378
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2014
    detail.hit.zdb_id: 1466401-X
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  • 6
    Online Resource
    Online Resource
    Abstract 15931: Glycogen Synthase Kinase-3α Plays a Critical Role in the Development of Cardiac Dysfunction During Obesity and Insulin Resistance Through Phosphorylation of Peroxisome Proliferator-Activated Receptor α
    Ovid Technologies (Wolters Kluwer Health) ; 2014
    In:  Circulation Vol. 130, No. suppl_2 ( 2014-11-25)
    Details
    In: Circulation, Ovid Technologies (Wolters Kluwer Health), Vol. 130, No. suppl_2 ( 2014-11-25)
    Abstract: Obesity and insulin resistance (IR) lead to impaired cardiac metabolism, resulting in cardiac dysfunction. However, the underlying mechanisms responsible for the development of cardiac dysfunction remain poorly understood. PPARα serves as a key regulator of fatty acid (FA) metabolism in the heart. GSK-3α, a serine/threonine kinase, was dephosphorylated at S21 and activated (2.0 fold, p 〈 0.05) in the hearts of obese mice fed a high-fat diet (HFD) and ob/ob mice. To evaluate the functional significance of GSK-3α upregulation, wild-type (WT) and cardiac specific GSK-3α heterozygous knockout (cGSK-3α HKO) mice were fed a HFD for up to 14 weeks. There was no difference in the food intake or body weight change between WT and cGSK-3α HKO mice. However, cardiac hypertrophy and diastolic dysfunction observed in WT mice were significantly ameliorated in cGSK-3α HKO mice after HFD feeding (8.1± 0.6 and 6.5±0.5, LVW/TL; 24.8±0.9 and 16.6±0.8, deceleration time (DT), all p 〈 0.05). FA oxidation (FAO) (0.81 fold) and ectopic lipid accumulation (Oil Red O staining) were significantly decreased in cGSK-3α HKO mice than in WT mice after HFD feeding. GSK-3α, but not GSK-3β, directly interacted with and phosphorylated PPARα at the ligand binding domain in cardiomyocytes (CMs) and in the heart. PPARα phosphorylation in the heart was significantly increased (2.1 fold, p 〈 0.05) in response to HFD, but it was attenuated in cGSK-3α HKO mice (0.74 fold, p 〈 0.05). Fenofibrate, a PPARα ligand, inhibited GSK-3α-induced PPARα phosphorylation (0.81 fold, p 〈 0.05), reduced ectopic lipid accumulation, FAO (0.84 fold, p 〈 0.05), and attenuated diastolic dysfunction (25.5±3.1 and 18.6±2.5, DT; 0.16±0.04 and 0.08±0.02, EDPVR, all p 〈 0.05) in the heart of HFD fed mice. Collectively, these results suggest that GSK-3α increases PPARα activity through phosphorylation of PPARα, which is inhibited by Fenofibrate. Activation of GSK-3α and consequent phosphorylation of PPARα during obesity and IR could play an important role in the development of cardiac hypertrophy and diastolic dysfunction. Synthetic PPARα ligands inhibit GSK-3α-mediated phosphorylation of PPARα, thereby paradoxically attenuating excessive FA metabolism in cardiomyocytes.
    Type of Medium: Online Resource
    ISSN: 0009-7322 , 1524-4539
    URL: Article
    DOI: 10.1161/circ.130.suppl_2.15931
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2014
    detail.hit.zdb_id: 1466401-X
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  • 7
    Online Resource
    Online Resource
    Persistent Stunning Induces Myocardial Hibernation and Protection : Flow/Function and Metabolic Mechanisms
    Ovid Technologies (Wolters Kluwer Health) ; 2003
    In:  Circulation Research Vol. 92, No. 11 ( 2003-06-13), p. 1233-1239
    Details
    In: Circulation Research, Ovid Technologies (Wolters Kluwer Health), Vol. 92, No. 11 ( 2003-06-13), p. 1233-1239
    Abstract: To test the hypothesis that persistent myocardial stunning can lead to hibernating myocardium, 13 pigs were chronically instrumented, and persistent stunning was induced regionally by 6 repetitive episodes of 90-minute coronary stenosis (CS) (30% reduction in baseline coronary blood flow [CBF]) followed by full reperfusion every 12 hours. During the 1st CS, CBF fell from 43±2 to 31±2 mL/min, and anterior wall thickening (AWT) fell by 54±8%, but posterior WT did not change. AWT never recovered fully and remained depressed by 31±7% before the 6th CS, reflecting persistent myocardial stunning, but baseline CBF was not changed. Surprisingly, during the 6th CS, AWT did not fall further despite a similar reduction in CBF during CS, as occurred with the 1st episode. Regional MV̇ o 2 fell similarly during the 1st and 6th CS. During the 1st CS, plasma glucose uptake increased, whereas free fatty acid (FFA) uptake was reduced. Before the 6th CS, glucose uptake remained elevated, whereas FFA uptake remained reduced. Histology revealed enhanced glycogen deposition, which could be explained by decreased glycogen synthase kinase (GSK)-3β protein levels and activity. These results indicate that persistent stunning, even in the absence of chronic ischemia, can recapitulate the phenotype of myocardial hibernation. This results in a shift in the flow/function relationship where a 30% decrease in CBF is no longer accompanied by a fall in myocardial function, which could be explained, in part, by a shift in substrate utilization. These hemodynamic/metabolic adjustments could facilitate survival of hibernating myocardium.
    Type of Medium: Online Resource
    ISSN: 0009-7330 , 1524-4571
    URL: Article
    DOI: 10.1161/01.RES.0000076892.18394.B6
    RVK:
    XA 10000
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2003
    detail.hit.zdb_id: 1467838-X
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  • 8
    Online Resource
    Online Resource
    Abstract 1257: Autophagy Plays Both Protective and Detrimental Roles in Post Myocardial Infarction Hearts
    Ovid Technologies (Wolters Kluwer Health) ; 2007
    In:  Circulation Vol. 116, No. suppl_16 ( 2007-10-16)
    Details
    In: Circulation, Ovid Technologies (Wolters Kluwer Health), Vol. 116, No. suppl_16 ( 2007-10-16)
    Abstract: Autophagy is an important mechanism of protein degradation involving formation of double membrane vesicles termed autophagosomes and lysosomal degradation. Autophagy is activated in the heart both under basal conditions and in response to stress. During acute ischemia, autophagy is protective, but during reperfusion, it may promote cell death, suggesting that the function of autophagy is context-dependent. In order to elucidate the role of autophagy in other pathological conditions in the heart, we examined whether autophagy is activated after myocardial infarction (MI) in vivo. On Day 2, autophagosome formation, as evaluated by GFP-LC3 dots, was significantly increased in the border zone compared with the remote area (25 vs 2 dots/field, p 〈 0.05, n=5). The functional significance of autophagy was evaluated using beclin 1 +/− mice, in which autophagy is significantly attenuated due to reduced expression of Beclin 1, a critical component of the autophagic machinery. Control (WT) and beclin 1 +/− mice (3 months old) were subjected to permanent coronary artery ligation. Kaplan Meier survival analyses indicated that the rate of mortality was significantly greater in WT (4 out of 13) than in beclin 1 +/− (0 out of 11) mice (p 〈 0.05) at early stages (0 –11 days), whereas there was no significant difference in mortality at later stages (11–29 days), suggesting that inhibition of autophagy is protective during early stages of MI. After 4 weeks, beclin 1 +/− mice exhibited larger LV myocyte cross sectional areas in remote areas (254 vs 220 μm 2 , p 〈 0.005) with greater posterior wall thickness (1.24 vs 1.11 mm, p 〈 0.05) and increased levels of cardiac myocyte apoptosis in the scar area (7.6 vs 2.8/mm 2 ) and the adjacent area (1.2 vs 0.6/mm 2 ) compared with WT mice. These results suggest that suppression of autophagy at late stages of MI promotes apoptosis and hypertrophy, and may be detrimental. In summary, autophagy is induced in the heart after MI and exhibits time-dependent functions. Although autophagy is detrimental at early (within 11 days) stages of MI, it may inhibit cardiac remodeling, and, thus, is protective during chronic stages.
    Type of Medium: Online Resource
    ISSN: 0009-7322 , 1524-4539
    URL: Article
    DOI: 10.1161/circ.116.suppl_16.II_256-a
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2007
    detail.hit.zdb_id: 1466401-X
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  • 9
    Online Resource
    Online Resource
    Abstract 20500: Trx1 Promotes Trans-Nitrosylation of Cellular Proteins to Stimulate Autophagy and Cell Survival
    Ovid Technologies (Wolters Kluwer Health) ; 2014
    In:  Circulation Vol. 130, No. suppl_2 ( 2014-11-25)
    Details
    In: Circulation, Ovid Technologies (Wolters Kluwer Health), Vol. 130, No. suppl_2 ( 2014-11-25)
    Abstract: Thioredoxin-1 (Trx1) is cardioprotective during oxidative stress, mainly through its antioxidant activity. Trx1 is also S-nitrosylated and, in turn, trans-nitrosylates other proteins. However, the role of Trx1-dependent S-nitrosylation in cardiomyocytes (CMs) is unknown. Here, we investigated the role of Trx1-mediated protein S-nitrosylation in the regulation of CM survival during stress in vitro. Using biotin-switch assays, we found that wild-type Trx1 (Trx1WT) is S-nitrosylated at baseline, but the extent of S-nitrosylation was attenuated in Trx1C73S, suggesting that Trx1 is S-nitrosylated at Cys73. Trx1WT and Trx1C73S do not differ in their redox activity, as determined by Amplex Red assays. Cellular protein S-nitrosylation levels were increased after 4 hours of glucose deprivation (GD), an energy stress condition (1.64±0.27 fold, p 〈 0.05), as determined by biotin switch assays. Overexpression of Trx1WT increased (3.94-fold), whereas knockdown of Trx1 (0.66±0.01 fold, p 〈 0.01) or overexpression of Trx1C73S (0.77±0.02 fold, p 〈 0.01) decreased, total protein S-nitrosylation in response to GD. These results suggest that Trx1C73 regulates protein S-nitrosylation in CMs during GD. Overexpression of Trx1 increased CM survival after 24 hours of GD (1.42±0.08 fold vs LacZ, p 〈 0.05), as evaluated with propidium iodide assays. Conversely, shTrx1 (2.13±0.05 fold vs control, p 〈 0.01) or Trx1C73S (1.73±0.034 fold vs LacZ, p 〈 0.01) increased cell death during GD. Either knockdown of Trx1 (LC3-II/Tubulin: 0.55 fold vs control) or overexpression of Trx1C73S (vs LacZ: LC3-II/Tubulin, 0.60 fold; autophagosomes, 0.83±0.16-fold, p 〈 0.005; autolysosomes, 0.62±0.13-fold, p 〈 0.005) significantly decreased autophagy during GD. Mechanistically, Trx1 co-immunoprecipitates with Atg7, an E1-like protein which plays a critical role in mediating autophagy. Using mass spectroscopy analyses, we found that SNO-Trx1 can trans-nitrosylate Atg7 in vitro. These results suggest that Trx1 trans-nitrosylates Atg7 during GD. Taken all together, our results indicate that Trx1 promotes trans-nitrosylation of cellular proteins, including Atg7, and autophagy, thereby promoting cell survival during energy stress in CMs.
    Type of Medium: Online Resource
    ISSN: 0009-7322 , 1524-4539
    URL: Article
    DOI: 10.1161/circ.130.suppl_2.20500
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2014
    detail.hit.zdb_id: 1466401-X
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  • 10
    Online Resource
    Online Resource
    Abstract 5362: Inhibition Of The Epidermal Growth Factor Receptor Transactivation By The Angiotensin II Type I Receptor Prevents Compensatory Cardiac Hypertrophy And Worsens Cardiac Function Following Myocardial Infarction
    Ovid Technologies (Wolters Kluwer Health) ; 2008
    In:  Circulation Vol. 118, No. suppl_18 ( 2008-10-28)
    Details
    In: Circulation, Ovid Technologies (Wolters Kluwer Health), Vol. 118, No. suppl_18 ( 2008-10-28)
    Abstract: The angiotensin II type I receptor (AT1R) has been shown to activate the epidermal growth factor receptor (EGFR). However, the downstream effects of this activation have not yet been elucidated in the heart. To examine the function of the AT1R-EGFR pathway, we have created an AT1R mutant in which amino acid 319 is mutated from tyrosine to phenylalanine (Y319F). The Y319F mutant lacks the ability to transactivate the EGFR. We generated transgenic lines overexpressing either wild type AT1R (Tg-WT) or Y319F (Tg-Y319F) only in the heart with similar levels of overexpression, and evaluated the contribution of the AT1R-EGFR pathway to cardiac responses against stress. Under baseline conditions at 3 months of age, cardiac function of Tg-WT and Tg-Y319F was not significantly different from non-transgenic mice (NTg) except that Tg-WT showed mild left ventricular hypertrophy. To examine the role of the AT1R-EGFR pathway under stress, we induced myocardial infarction (MI) by permanently ligating the left anterior descending coronary artery. Four weeks after MI, increases in heart weight/tibia length (Tg-WT, Tg-Y319F, NTg: 12.57, 10.11, 9.96, p 〈 0.05 vs Tg-WT) and left ventricular myocyte cross sectional area (35, 5, 29% vs sham, p 〈 0.05) were significantly attenuated in Tg-Y319F compared to Tg-WT. Fibrosis was also milder in Tg-Y319F than in Tg-WT (10.7% vs 22.9%). These results suggest that the AT1R-EGFR pathway plays an important role in mediating LV hypertrophy and fibrosis after MI. Interestingly, however, echocardiographic measurement showed that Tg-Y319F have impaired LV ejection fraction (Tg-WT, Tg-Y319F, NTg: 51, 19, 44%, p 〈 0.05) and %fractional shortening (21.4, 6.7, 17.7%, p 〈 0.05) compared with Tg-WT or NTg. Tg-Y319F showed an increase in mortality in days 0–28 following MI, when compared to Tg-WT and NTg (35, 67, 30%, p 〈 0.5). Additionally, lung weight/tibia length was increased in Tg-Y319F (11.3, 24.7, 16.1, p 〈 0.05) These results suggest that the lack of EGFR activation causes cardiac dysfunction after MI. In summary, transactivation of the EGFR following MI may play a compensatory role, thereby protecting the heart from further deterioration of cardiac function. This research has received full or partial funding support from the American Heart Association, AHA Founders Affiliate (Connecticut, Maine, Massachusetts, New Hampshire, New Jersey, New York, Rhode Island, Vermont).
    Type of Medium: Online Resource
    ISSN: 0009-7322 , 1524-4539
    URL: Article
    DOI: 10.1161/circ.118.suppl_18.S_535-b
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2008
    detail.hit.zdb_id: 1466401-X
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